Evaluation of moecules termed UBCs and E3s as targets for cancer therapy

Lead researcher

Dr Borislav Sarcevic

InstitutionSt Vincent's Institute of Medical Research

Years funded2007

Research into the treatment of cancer in people of all ages. Unrestrained cell proliferationis a primary characteristic of cancerous cells and hence understanding the causes of increased cellular division is fundamental to understanding the development of cancer. In addition to increasing our knowledge of cancer, defining the underlying molecular mechanisms of growth control in cancer will be required to develop new therapies for cancer treatment. A highly successful example of this is the use of tamoxifen to treat breast cancer by inhibiting the growth promoting effects of estrogen on breast cancer cells. The identification of new growth pathways and targets is required to develop new therapies. It is now well established that the increased activity of molecules directly involved in causing cell division or decreased activity of molecules involved in inhibiting cell division is intimately involved in the development of many human cancers. We have discovered a region on a class of molecules important for regulating cell division termed, UBCs and E3s, which is critical for their activity. Some of these molecules are overactive in human cancers such as breast cancer. Our studies suggest that this region may be a good target for the development of drugs to inhibit these molecules and their effects on cancer cell growth. We will evaluate this by introducing modified variants of these molecules inside actively growing cells and assessing if they regulate the rate of cellular growth. Ultimately, these studies will identify if these molecules may be potential therapeutic targets in the treatment of cancer.

Cancer Council Victoria would like to acknowledge the traditional custodians of the land on which we live and work. We would also like to pay respect to the elders past and present and extend that respect to all other Aboriginal people.